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1 inward rectifier, plus SUR2A, a low-affinity sulfonylurea receptor.
2 or family, in keeping with the presence of a sulfonylurea receptor.
3 enzymes, beta-cell-specific glucokinase and sulfonylurea receptor.
4 ATP-sensitive K(+) (K(ATP)) channels is the sulfonylurea receptor.
5 inwardly rectifying Kir channel (Kir6.x) and sulfonylurea receptors.
6 nnels, with SUR 1 and SUR 2, probably SUR2B, sulfonylurea receptors.
8 otassium (K(ATP)) channel, a complex of four sulfonylurea receptor 1 (SUR1) and four potassium channe
9 ABCC8 and KCNJ11, which encode the subunits sulfonylurea receptor 1 (SUR1) and inwardly rectifying p
10 tive potassium (K(ATP)) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2 regulate insul
11 h defects in ABCC8 and KCNJ11 genes encoding sulfonylurea receptor 1 (SUR1) and Kir6.2 subunits, whic
12 ATP-sensitive K(+) (K(ATP)) channel proteins sulfonylurea receptor 1 (SUR1) and Kir6.2, encoded by AB
13 caused by mutations in the channel proteins: sulfonylurea receptor 1 (SUR1) and Kir6.2, results in lo
16 ensitive potassium (K(ATP)) channel subunits sulfonylurea receptor 1 (SUR1) and the inwardly rectifyi
17 tive potassium (KATP) channels consisting of sulfonylurea receptor 1 (SUR1) and the potassium channel
18 ed glucose sensitivity after deletion of the sulfonylurea receptor 1 (SUR1) both in man and mouse.
19 outward current that was antagonized by the sulfonylurea receptor 1 (SUR1) channel blocker tolbutami
21 tions in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifyin
22 tudies using transfected COSm6 cells, mutant sulfonylurea receptor 1 (SUR1) protein was expressed on
23 s to nucleotide binding fold-1 (NBF1) of the sulfonylurea receptor 1 (SUR1) subunit of the KATP chann
26 in ischemic astrocytes that is regulated by sulfonylurea receptor 1 (SUR1), is opened by depletion o
28 scovery of a disease-causing mutation in the sulfonylurea receptor 1 (SUR1)/ABCC8 from a patient with
31 ns in ABCC8 or KCNJ11, genes that encode the sulfonylurea receptor 1 or the inward rectifier Kir6.2 s
32 ATP-sensitive K(+) channel (K(ATP) channel) sulfonylurea receptor 1 subunit, and decreased inhibitor
33 ying potassium channel Kir6.2 assembles with sulfonylurea receptor 1 to form the ATP-sensitive potass
34 cases are associated with mutations in SUR1 (Sulfonylurea receptor 1) or KIR6.2 (Inward rectifier K(+
35 Kir6.2 or its associated regulatory subunit, sulfonylurea receptor 1, causes congenital hyperinsulini
36 K(ATP) channel, a functional complex of the sulfonylurea receptor 1, SUR1, and an inward rectifier p
37 cervical SCI, we tested the hypothesis that sulfonylurea receptor 1-regulated (SUR1-regulated) Ca(2+
39 inemic hypoglycemia, similar channel loss in sulfonylurea receptor-1 (SUR1) and Kir6.2 null mice yiel
41 There was no association between mean/peak sulfonylurea receptor-1 and mean/peak intracranial press
43 is available, assessing cerebrospinal fluid sulfonylurea receptor-1 in larger studies is warranted t
53 nes were generated and independently bred to sulfonylurea receptor 2 (SUR2) null mice to generate mic
54 tations in the genes encoding the regulatory sulfonylurea receptor 2 (SUR2) subunits of the ATP-sensi
56 T-PCR) using primers specific for Kir6.2 and sulfonylurea receptor 2A (SUR2A) subunits was performed
59 kidney 293 cell-attached patches expressing sulfonylurea receptor 2B and Kir6.2, we found K(ATP) sti
60 ed equivalent of this channel comprising the sulfonylurea receptor 2B and the inward rectifier 6.1 su
62 in the second nucleotide-binding fold of the sulfonylurea receptor, a subunit of the pancreatic-islet
63 iant in the gene encoding a component of the sulfonylurea receptor (ABCC8 p.A1369S) promotes closure
65 l beta-cells, including rat insulin, amylin, sulfonylurea receptor, and glucokinase, are stably expre
66 both nucleotide-binding-fold regions of the sulfonylurea receptor are required for normal regulation
67 Superfusion of tolbutamide, a K(ATP) channel sulfonylurea receptor blocker, elicited identical glucos
68 a transgenic strategy where the full-length sulfonylurea receptor containing exon 40 was expressed u
69 osinophils do express mRNA homologous to the sulfonylurea receptor family, in keeping with the presen
72 lurea 1 and 2 failed to show expression of a sulfonylurea receptor in the parietal cell, thus further
77 ce probe BODIPY-FL-glyburide labeling of the sulfonylurea receptor of mitoK(ATP) from brain and liver
78 ct with ABC proteins beyond the subfamily of sulfonylurea receptors provides an intriguing explanatio
79 inwardly rectifying potassium channel and a sulfonylurea receptor regulatory subunit (SUR1 or SUR2).
80 yeast cadmium resistance transporter and the sulfonylurea receptor share a conserved topology disting
83 pore-forming subunit (Kir6.2) but different sulfonylurea receptor subunits (SUR1 and SUR2A, respecti
84 r6.2 subunits complexed with four regulatory sulfonylurea receptor subunits (SUR1 in pancreatic beta-
85 ed from pore-forming (Kir6.x) and regulatory sulfonylurea receptor subunits, are critical electrical
86 , an inwardly rectifying K+ channel, and the sulfonylurea receptor SUR, an ATP binding cassette prote
87 e components of KATP channels in beta-cells, sulfonylurea receptor (SUR) 1 and Kir6.2, have operation
88 he ATP-gated K(+) (K(ATP)) metabolic sensor [sulfonylurea receptor (SUR) 1 and potassium inwardly rec
89 rd rectifier potassium channel (Kir) 6.2 and sulfonylurea receptor (SUR) 1 critically regulate pancre
92 eter regulation of wild-type [SUR2(+/+)] and sulfonylurea receptor (SUR) 2-deficient [SUR2(-/-)] mous
97 timeric structures formed by a member of the sulfonylurea receptor (SUR) family and a member of the i
102 second nucleotide-binding fold (NBF2) of the sulfonylurea receptor (SUR) of an individual diagnosed w
103 a member of the ATP binding cassette family (sulfonylurea receptor (SUR) or cystic fibrosis transmemb
104 e KATP channel is formed from four each of a sulfonylurea receptor (SUR) regulatory subunit and an in
105 el subunit (Kir6.1, Kir6.2) and a regulatory sulfonylurea receptor (SUR) subunit, an ATP-binding cass
106 ATP), channels are comprised of K(IR)6.x and sulfonylurea receptor (SUR) subunits that assemble as oc
109 ssion of the inward rectifier Kir6.2 and the sulfonylurea receptor (SUR), a member of the ATP-binding
111 transmembrane conductance regulator (CFTR), sulfonylurea receptor (SUR), and heavy metal tolerance f
112 rectifying K(+) channel 6.2 (Kir6.2) and the sulfonylurea receptor (SUR), now renamed SUR1, subunits
113 -dependent stimulatory action of the ATPase, sulfonylurea receptor (SUR), on K(IR) sufficient to elic
120 novo L225P mutation in the L0 region of the sulfonylurea receptor (SUR)1, the regulatory subunit of
121 sized that the mitoK(ATP) channel contains a sulfonylurea receptor (SUR)2 regulatory subunit and aime
123 els (K(ATP) channels) are heteromultimers of sulfonylurea receptors (SUR) and inwardly rectifying pot
124 mponent gene expression including regulatory sulfonylurea receptors (SUR) SUR1 and SUR2B but not SUR2
125 channels are heteromultimers of KIR6.2 and a sulfonylurea receptor, SUR, an ATP binding cassette (ABC
126 s tissues contain subtypes of the regulatory sulfonylurea receptor, SUR, and pore-forming, K(+) inwar
127 itive potassium (K(ATP)) channel composed of sulfonylurea receptor SUR1 and potassium channel Kir6.2
129 ective opener for K(ATP) channels containing sulfonylurea receptor SUR1 subunits, but not with cromak
131 , is composed of two types of subunits: 1) a sulfonylurea receptor (SUR1) and 2) an inwardly rectifyi
132 are an octameric assembly of two proteins, a sulfonylurea receptor (SUR1) and an ion conducting subun
133 channel, composed of the beta-cell proteins sulfonylurea receptor (SUR1) and inward-rectifying potas
135 probands were screened for mutations in the sulfonylurea receptor (SUR1) gene by single-strand confo
137 l membranes indicated that the high affinity sulfonylurea receptor (SUR1) is not present on eosinophi
138 tween them and a nearby pancreatic beta-cell sulfonylurea receptor (SUR1) missense variant (S1370A),
139 complex of pore-forming Kir6.2 subunits and sulfonylurea receptor (SUR1) subunits with two nucleotid
144 no evidence for the presence of either known sulfonylurea receptors (SUR1 or SUR2) in the mitochondri
145 mily (Kir6.1, KCNJ8, and Kir6.2 KCNJ11) with sulfonylurea receptors (SUR1, ABCC8, and SUR2, ABCC9) of
146 l KATP (surfaceKATP) channels encoded by the sulfonylurea receptor SUR2A and the pore-forming subunit
147 rmed from pore-forming Kir6.2 and regulatory sulfonylurea receptors (SUR2A in heart and skeletal musc
149 rvations and the unexpected partnership with sulfonylurea-receptors (SURs) makes the TRPM4 channel a
151 K(ATP) channels are formed as a complex of a sulfonylurea receptor (SURx), a member of the ATP-bindin
156 osynthesis and were thought to interact with sulfonylurea receptors that mediate chitin vesicle trans
157 rough association of the Kir6.2 pore and the sulfonylurea receptor, the stress-responsive ATP-sensiti
159 ; however, the evidence is strong that SUR1 (sulfonylurea receptor type 1) subunits are also expresse
161 -rectifier potassium channel 6.2) and SUR2A (sulfonylurea receptor type 2A) subunits; however, the ev
163 ic ATP-binding cassette regulatory subunits (sulfonylurea receptors), which counterbalance the nearly
164 The gene responsible (SUR1) encodes the sulfonylurea receptor, which maps to chromosome 11p15.1.
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